Tachycardia, the term referring to abnormally high heart rate, includes conditions such as tachycardiac arrhythmias, in which case an affected chamber of the heart (ventricle or atrium) contracts in an orderly manner, although at a physiologically inappropriately high rate. In the case of fibrillation, however, a heart chamber contracts in a disorderly manner due to circulating excitation, and the affected heart chamber basically no longer assists in pumping blood volume. Ventricular fibrillations (VF) can therefore be fatal. If they are detected quickly and reliably, they can be terminated using a defibrillation shock from a defibrillator.
Implantable cardiac stimulators in the form of cardiac pacemakers or implantable cardioverters/defibrillators (ICDs) are well known. Such cardiac stimulators are typically connected to electrode leads which include stimulation or defibrillation electrodes in or near a heart chamber. A cardiac pacemaker can use a stimulation electrode to deliver an electrical stimulation pulse to the muscle tissue of a heart chamber to thereby induce a stimulated contraction of the heart chamber, provided the stimulation pulse has sufficient intensity and the cardiac muscle tissue (myocardium) is not in a refractory phase at the moment. Electrode leads including stimulation electrodes having relatively small surface areas are typically used to trigger a stimulated contraction of a heart chamber in this manner, since the initial stimulation of only a small portion of the myocardium of the heart chamber is sufficient to trigger a stimulated contraction. Such a stimulated contraction of a heart chamber is referred to in this document as a “stimulated” event. If a natural contraction of the heart chamber occurs, this is referred to as a “natural” or “intrinsic” event. For example, a contraction of the right atrium of a heart may be referred to as an atrial event, which can be a natural (or intrinsic) atrial event, or where triggered by an atrial cardiac pacemaker or similar device, can be a stimulated atrial event. Similar distinctions can be made between natural (intrinsic) and stimulated left ventricular events and right ventricular events.
A local excitation of the myocardium propagates from the excitation site by conduction in the myocardium, resulting in depolarization of the muscle cells and thus contraction of the myocardium. After a short period of time the muscle cells are repolarized and the myocardium therefore relaxes. During the depolarization phase, the cardiac muscle cells are insensitive to excitation, i.e. they are refractory. The electrical potentials associated with depolarization and repolarization can be sensed, and the course thereof over time—referred to as an electrocardiogram—can be evaluated. In the electrocardiogram, a so-called R peak represents a depolarization of the ventricular myocardium and therefore a contraction of the ventricle. The repolarization of the ventricular myocardium is expressed as a so-called T wave. These signal features can be detected automatically using an appropriate sensing unit, typically by comparing signal values with threshold values. When this is done, a T wave can exceed the threshold value for detecting R peaks, and therefore a T wave is incorrectly identified as an alleged R peak. This phenomenon is referred to as T wave oversensing.
Such natural (intrinsic) events are detected by determining the electrical potentials of the myocardium of a selected heart chamber using sensing electrodes which are part of a corresponding electrode lead. The sensing electrodes can also serve as stimulation electrodes, wherein the electrodes alternate between stimulation and sensing functions (i.e., delivery and detection of potentials). Typically, a pair of electrodes composed of a tip electrode and a ring electrode is provided for the sensing, wherein the tip electrode is also used as the stimulation electrode. A bipolar recording of an intracardiac electrocardiogram (IEGM) is obtained in this manner. In that case, sensing and stimulation take place in the ventricle using a ventricular electrode lead, and stimulation and sensing take place in the (right) atrium using an atrial electrode lead which is separately connected to the cardiac stimulator. If a left ventricular electrode lead is also provided, it typically extends via the coronary sinus and a lateral vein branching off therefrom into the vicinity of the left ventricle, where it can include a stimulation electrode and/or sensing electrode having a small surface area.
During operation of the cardiac stimulator, the sensing electrodes are connected to appropriate sensing units which are designed to evaluate a recorded electrocardiogram using a sensing electrode (or a pair of sensing electrodes), and, in particular, to detect intrinsic atrial or ventricular events, i.e. natural atrial or ventricular contractions. This takes place, for example, by comparison with a threshold value, i.e. an intrinsic event is detected when a particular intracardiac electrocardiogram exceeds a suitably specified threshold value. Sensing units, which are connected to intracardiac electrodes during operation, are typically provided in an implantable cardiac stimulator for the detection of intrinsic events.
So-called blanking periods and refractory periods are typically provided during the course of sensing intrinsic events. A blanking period is started once an R peak is detected, to prevent the same event from being detected twice. No events are sensed during the blanking period. When an R peak is detected, a refractory period is also started, during which intrinsic events are sensed (outside of the blanking period), but are not detected as such. If the refractory period is dimensioned such that it extends beyond the moment when a T wave is expected, such a T wave is not detected as an intrinsic event (contraction of the heart chamber).
The intrinsic atrial heart rate (atrial frequency) or ventricular heart rate (ventricular frequency) can be derived from the frequency at which the atrial and ventricular events follow one another, thus enabling the detection of tachycardias, for example. T wave oversensing is a problem here, since T wave oversensing can suggest the alleged presence of tachycardia.
The invention assists with improving the detection of ventricular fibrillation (VF) in combination with good suppression of T wave oversensing. The solution is particularly advantageous for VF signals having significantly fluctuating amplitudes.
Input stages of modern implantable cardioverter/defibrillators (ICDs) or cardiac stimulators for cardiac resynchronization therapy (CRT-Ds) already provide algorithms for the automatic adaptation of sensing thresholds to the signal conditions. However, they typically utilize sensing thresholds that derived from measured signal amplitudes. Furthermore, to blank the T wave after detection of an R wave, a so-called upper threshold (e.g. 75% of the R wave amplitude) is often used, which is then switched to a lower threshold (e.g. 25%) after the expected duration of the T wave (e.g. after 360 ms). The result is that the T wave can be blanked in that it remains below the threshold, yet smaller fibrillation waves can then be detected using the subsequently activated lower threshold.
Typical methods have the disadvantage that fibrillation waves having greatly fluctuating amplitudes cannot be adequately sensed by using a so-called upper threshold of 75%, for example, for a period of 360 ms. However, if the upper threshold is set lower (e.g. 50%), a large T wave cannot be blanked, and so patients with large T waves are at risk of limited VF sensing.